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[细胞外基质、基质降解蛋白酶与血管钙化]

[Extracellular matrix, matrix-degrading proteases and vascular calcification].

作者信息

Du Yao-Yao, Wang Xian, Kong Wei

机构信息

Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100083, China.

出版信息

Sheng Li Ke Xue Jin Zhan. 2008 Jul;39(3):203-8.

PMID:18819486
Abstract

Vascular calcification is a common phenomena among atherosclerosis, diabetes, chronic kidney failure and aging. Recently, extensive researches have shown that the mechanisms of vascular calcification share great similarity with physiological mineralization rather than a passive deposition of calcium and phosphate. As a major component of blood vessels, the extracellular matrix (ECM) proteins not only provide a scaffold for normal vasculature, but also regulate the attachment, proliferation, migration and differentiation of vascular cells through ECM-cell interaction. Furthermore, it also serves as a reservoir for growth factors or cytokines. Previous studies have indicated the potential importance of ECM and ECM degrading proteases during vascular calcification. Extracellular matrix not only provides a major site for calcium and phosphate deposition, but also actively participates in the process of calcification through an accelerating or inhibitory effect. Multiple extracellular matrix proteins have been altered during the calcification. The disturbance of the delicate balance of ECM homeostasis may affect the evolution of vascular calcification. On the other hand, matrix degrading proteases (such as MMPs) may be involved in the occurrence and development of vascular calcification by affecting matrix or non-matrix substances (such as cytokines or growth factors). The current review summarizes the recent advance on vascular calcification in the context of ECM and MMPs.

摘要

血管钙化是动脉粥样硬化、糖尿病、慢性肾衰竭及衰老过程中常见的现象。最近,大量研究表明,血管钙化机制与生理性矿化有很大相似性,而非钙和磷的被动沉积。作为血管的主要组成部分,细胞外基质(ECM)蛋白不仅为正常血管提供支架,还通过ECM-细胞相互作用调节血管细胞的黏附、增殖、迁移和分化。此外,它还作为生长因子或细胞因子的储存库。先前的研究表明ECM和ECM降解蛋白酶在血管钙化过程中具有潜在重要性。细胞外基质不仅为钙和磷沉积提供主要场所,还通过促进或抑制作用积极参与钙化过程。在钙化过程中多种细胞外基质蛋白发生了改变。ECM稳态的微妙平衡受到干扰可能会影响血管钙化的发展。另一方面,基质降解蛋白酶(如基质金属蛋白酶)可能通过影响基质或非基质物质(如细胞因子或生长因子)参与血管钙化的发生和发展。本综述总结了在ECM和基质金属蛋白酶背景下血管钙化的最新进展。

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